Chapter 5 Nonopioid Analgesics THIS ONE
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Transcript of Chapter 5 Nonopioid Analgesics THIS ONE
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Premedication Regimen
No allergy to Penicillin
2g or 2000mg Amoxicillin one hr prior to
appt time
RX:
Amoxicillin 500mg caps
Dispense 4
Take four capsules 1 hour before appointment
time.
Refills Zero
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Premedication Regimen
Allergy to Penicillin
600mg Clindamycin
Available in 150 mg or 300mg capsules RX:
Clindamycin 150 mg capsules
Take 4 caps 1 h before appointment time. Refills Zero
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Nonopioid (Non Narcotic)
AnalgesicsChapter 5
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Pain
Pain is the means by which the body ismade urgently aware of the presence oftissue damage. Suffering or distress of
the body and or mind.
Protective reflex for self-preservation
Diagnostic symptom of an underlyingpathologic condition
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Pain
Pain Control is of great importance in the
dental office
Pain brings patient to the dental office
Conversely, pain will keep patient away from the
dental office
Provider needs to recognize and evaluate
a patients need for medication
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Two components of pain
Perceptionphys ical componentof pain
Involves the message of pain that is
carried through the nerves eventually tothe cortex.
Reaction psycho logical component
of pain, involves the patients emotionalresponse to the pain.
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Pain Threshold
Individuals perceive pain but reactdifferently to it.
Decrease in pain threshold-greater
reaction to pain. Decrease in PT associated with emotional
instability, anxiety, youth, fatigue, certain
nationalities, women, fear, andapprehension.
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Raise Pain Threshold
Getting adequate sleep
Sympathy-understanding
Activities-hold a pts hand, talk with thepatient, stay busy, swim, hot shower,
meditation, etc..
Analgesics- Tylenol, Advil, Motrin, Aspirin
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Pain Threshold
Analgesic therapy must be selected for the
individual
A level of discomfort that may not require
drug treatment in one person may demand
extreme therapy in another
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Classification of Analgesic Agents
Divided into 2 groups
1-Nonopiods-aka: nonnarcotic,
peripheral, mild, and antipyretic,
analgesics.
Site of action-peripheral nerve endings,
mediated centrally
2-Opiods-aka: narcotic central, or strong
group.
Site of action-act primarily on the central
nervous system
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More Actions
Action of non-opioid analgesics related to
theirability to inhibit prostaglandin
synthesis
Opioids affect the response to pain by
depressing the CNS
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Non-Opioids
Non-opioids are divided into:
salicylates (aspirin-like) i.e Anacin,
Diflunisal
acetylsalicylic acid (ASA)
acetic acid and salicylic acid
acetic acid imparts the vinegar odor to a
bottle of aspirin when it gets old
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Non-Opioids
acetaminophen (Tylenol)
NSAIDs (nonsteroidal anti-inflammatory
drugs/agents) i.e. Advil, ibuprofen,
Naproxen, Etodolac, Ketoprofen
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Salicylates
From extracts of willow bark and containsalicin that have been used to reduce
fever
Chemical name: acetylsalicylicacid=ASA=aspirin
ASA HA(acetic acid) + SA(salicytic acid)
Acetic acid has characteristic of vinegarodor = ifyour bottle of aspirin STINKS,
then it is time for a new one
Metabolized via zero order kinetics
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Acetylsalicylic Acid
Mechanism of Action
Analgesic - pain reliever
Better to give before pain begins, effectiveagainst throbbing pain vs. a stabbing pain.
Inhibits prostaglandin synthesis Inhibits enzyme cyclo-oxygenase (COX or COX II)
What types of procedures or dental problemscome to mind when you hear a patient saythrobbing pain? Stabbing pain?
A t l li li A id
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Acetylsalicylic Acid
Mechanism of Action
What are prostaglandins?
From arachidonic acid
Are lipids that are synthesized locally by
inflammatory stimuli
Sensitize pain receptors to bradykinin
Bradykinin has two receptors
B1 involved with tissue injury, chronic pain andplays a role with inflammation
A t l li li A id
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Acetylsalicylic Acid
Mechanism of Action
aspirin blocks the synthesis of
prostaglandins
Effective if given before painful stimuli are
experienced
More effective against throbbing pain
Due to inflammation
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Acetylsalicyclic Acid
Mechanism of Action Antipyretic - fever reducer-induces
peripheral vasodilation and sweating
Reduces prostaglandin synthesis in the
hypothalamus The higher the prostaglandin synthesis the higher
the body temp
Anti-inflammatory- inflammation reducer
(by inhibiting prostaglandin synthesis) Prostaglandins strong vasodilators-capillary
permeability
aspirin decreases erythema and swelling
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Acetylsalicyclic Acid
Mechanism of Action
Anti-platelet effects blood thinner
Irreversibly binds to platelets and reduces
platelet adhesivenessAll platelets affected (will not normally clot)
New platelets will need to form (4-7 days)
After 20% of platelets replaced normal clotting
returns (about 36 hours)
Taken orally absorbed in small intestine
ASA (cont)
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ASA (cont) Reaches peak effect
on empty stomach in
30 minutes Buffered tablet in 20
minutes- buffer will
help the aspirin be
dispersed, and
dissolved quicker, it
has higher blood
levels Buffer = slower
absorption but that is
offset by the faster
rate of dissolution
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ASA (cont) Given orally or rectally
Never apply directly to tooth or mucosa =painful ulceration
Take when MI is suspected
GI effects (most frequent effect)-nausea,vomiting, gastric irritation, may exacerbatepreexisting ulcers, gastritis, or hernia
Antacids reduce absorption with diflunisal Metabolized in the liver
Excreted by the kidney
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ASA common drug reactions warfarin (Coumadin)=bleeding
Methotrexate (cancer drug)
probenecid (gout medicine)
Interferes with ACE inhibitors, beta blockers,
reducing antihypertensive effects Dosage for aspirin
Fever = 325 to 650mg every 4 hours
Arthritis = between 3-6gm a day
LD for pediatrics 4 gm, adults 10-30 gm
Enteric-Coated Aspirin-coat dissolves in the
intestine rather than the stomach
Aspirin with caffeine is more effective
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ASA common drug reactions and
contraindications
Inhibits prothrombin production resulting inhypoprothrombinemia
In children and adolescentsassociated withReyes Syndrome when taken for chicken poxand influenza. (use Tylenol instead)
No use during pregnancy
Allergy=usually occurs in asthmatics Nasal polyps, asthma, and aspirin
hypersensitivity
Triad usually occurs
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ASA common drug reactions
and contraindications
True allergy to aspirin is uncommon
Toxic levels taken=salicylismtinnitus,
headache, dizziness, dimness of vision,electrolyte imbalance, hyperthermia
All meds should be in childproofcontainers
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ASA common drug
combinations
Can add to a sedative, but preferred to
prescribe separately for more control
Mix with another opioid can allow a
decrease in the amount of opioid in the
product and reduce side effects
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diflunisal (Dolobid)
Advantages-thought to have no effect onplatelets and no cross-hypersensitivity withaspirin
Fewer GI side effects (not much proof of) Contain magnesium, contraindicated in
renal disease
This is a salicylate classified as anNSAID
Premed with this to delay post op pain
Given 2-3x/day; no useful antipyretic effect
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diflunisal (Dolobid)
Classified as an NSAID
Peak action 2-3 hrs after ingestion
Not recommended for acute dental pain
May take before dental pain
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NSAIAs or NSAIDs
Brand Names
Generic
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Nonsteroidal Antiinflammatory
Agents
Kissin cousins of aspirin ??Most useful drug group for tx of dental
pain
Classified by chemical make-up/Name(pg. 57)
Common Rx for pain = propionic acid
derivitives-naproxen sodium (Anaprox)
-naproxen (Naprosyn)
-ibu rofen Advil, Motrin
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NSAIDs
Some other commonly used derivatives:
Acetic acid derivatives
indomethacin (Indocin)
etodolac (Lodine)
diclofenac (Voltaren)
Salicylates (but classified as a NSAID)
diflunisal (Dolobid) Oxicams
proxicam (Feldene)
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Mechanism of Action
Inhibit prostaglandin synthesis by inhibiting
the enzyme COX COX I and II
ibuprofen (Advil)
naproxen (Naprosyn, Aleve)
meclofenamate (Meclomen)
COX I specific
indomethacin
COX II
celecoxib (Celebrex)
Most peak in 1-2 hours
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Mechanism of Action
Take with food to reduce the rate of
absorption
Antacids have no effect on absorption except
diflunisal
Used as an analgesic, anti-inflammatory,
antipyretic, especially rec. for menstrual
cramps (dysmenorrhea)
Metabolized in the liver
Excreted via kidneys
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Mechanism of Action
Tissue Injury TriggersCOXII in periphery
tissue
COXII will convertarachidonic acid toprostaglandin E2
(PGE2)
Results in stimulationof the nociceptor inperipheral nerve to
send a signal for painin the CNS
A nociceptor is a sensory receptor that sends
signals that cause the perception of pain in
response to potentially damaging stimulus
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Adverse Reactions
GI irritation, pain, bleeding, increase acid
secretion
CNS-vertigo, headache, depression,
convulsions
These are not addicting, no tolerance, no
withdrawal
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Adverse Reactions
Reversibly inhibit platelet aggregation:
Effect lasts as long as med in blood
No need to wait for new platelets to form
ibuprofen in the blood 1 day
naproxen 4 days
oxaprozin 2 weeks
Adverse reactions (cont)
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Adverse reactions (cont)
Cause Lithium toxicity, increase effect of
digoxin ( used for heart failure), reduceseffects forB-blockers, ACE inhibitors
and diuretics
Hypersensitivity-hives, itching, chills, fever Dry mouth, gingival ulcerations
Renal effects
Contraindicated for pregnancyprolongsgestation (Category C)
Use with caution in pt.s with renal and
hepatic conditions, sens. to aspirin
Therapeutic Uses
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Therapeutic Uses
Osteoarthritis, pain, fever, dysmenorrhea
Manage dental pain Take with full glass of water, and food
Use caution when driving
Do not use with aspirin Do not take OTC analgesics with Rx
NSAIAs
If pain does not subside call DDS
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Specifics on NSAIDs - ibuprofen Ibuprofen (Advil, Motrin)
-onset 30 mins, duration2-4 hrs.
-metabolized in liver,
excreted by kidneys
-Drug of choice for dental
pain
-400-800mg every 4-6
hrs.-do not exceed 3200mg
in a 24 hour period
- dose = anti-inflam.
-200mg capsules,
tablet = OTC
-400, 600, 800mg = Rx-more effective than
ace. with codeine,
-double doses of ace.
C I hibit
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Cox Inhibitors
Specific Cox II inhibitors block the enzyme
that is synthesized when inflammationoccurs
-Celebra, Celebrex (lowest dose
possible)(higher GI upset), refecoxib(Vioxx) and valdecoxib (Bextra) (off the
market) (arthritis)
Cox I-widely distributed, always presentenzyme
-responsible for adverse effects of
NSAIDs.
N d N
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Naproxen and Naproxen
Sodium Proprionic acid derivative NSAID
Slightly longer half lives
Dosed on an 8-12 hour schedule Longer acting
Need loading dose
naproxen 500 mg stat; 250 mg q 6-8; max
daily = 1500mg (peaks in 2-4h)
naproxen sodium 550mg stat;275 mg q6-8h
daily max = 1375 (peaks in 1-2h)
Will cause lithium levels to rise
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ACETAMINOPHEN
USES
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USESANALGESIC AND ANTIPYRETIC
PT WITH ASPIRIN SENSITIVITY PT WITH GI UPSET FROM ASPIRIN
YOUNG CHILDREN
Dose 1-2 tabs/caps (325 to 650mg) every4 -6 hours OR 1000mg -3-4 X/day
FDA does not recommend more than 650mg every 4-6 hours, 3-4X/day
4000mg/day
New recommended single dose
Must include a box warning mostdangerous type for liver failure
USES
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USES
Dose 1-2 tabs/caps (325 to 650mg) every4 -6 hours OR 1000mg -3-4 X/dayDo notgive to children
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Ph l i Eff t
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Pharmacologic Effects Rapidly absorbed form GI
Peaks in 1-3 hours Large doses produce a metabolite in liver
that can be hepatotoxic and nephrotoxic
Equally efficacious as aspirin (pain) andjust as potent for fever and pain.
Alcoholics avoid acetominophen
No effect on resp. or CV. No GI bleeding Does not produce or affect platelet
adhesiveness, or uric acid excretion
Ph l i Eff t
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Pharmacologic Effects
Acetaminophen and AlcoholAlcohol stimulates oxidizing enzymes that
metabolize acetaminophen to its TOXICMETABOLITE
Normal maximum dose for people who DONOT drink = 325 per pill x2 = 650 mgevery 4 - 6 hours
For moderate drinkers (< 3 drinks a day),do not exceed 2gm of acetaminophen
For people who exceed 3 drinks a day orsomeone is an alcoholic AVOID
ACETAMINOPHEN
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DRUGS USED TO TREATGOUT URICOSURIC EFFECT
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GOUT
Inherited disease
Primarily in men
Involves one joint
Often big toe or knee Hyperuricemia and urate crystals are found at
joints (amount of uric acid)
Uric acid must be excreted because it cannot be
destroyed within the body Excess acid caused by excessive production
or reduced ability to excrete adequate amount ofuric acid
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GOUT
Colchicine
Treatment of an acute
case of gout
Taken hourly at theonset
Interferes with
inflammatory response
Side effects Vomiting
Diarrhea
Nausea
allopurinol (Zyloprim)
Inhibits synthesis of
uric acid
Prevent excess fromforming
Used with patients in
chemotherapy
Death of cells release
uric acid
D U d t T t G t
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Drugs Used to Treat Gout
Gout-inherited disease, mostly men,
involves 1 joint (big toe, knee, elbow) probenecid (Benemid) and allopurinol
used to prevent gout but have no pain
relief Due to an excess or uric acid (produce too
much or do not excrete enough)
Colchicine - on ly usedto tx attack of gout-taken hourly at the onset of attack
-most common side effect = GI
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Gout (cont)
allopurinol (Zyloprim)-
inhibits the synthesis
of uric acid
Also used to tx. pts
receiving chemo,
death of cells cause a
release of uric acid
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Gout (cont)
probenecid (Benemid)
increase excretion of
uric acid
GI effects, sore
gums,
Increases levels of
NSAIDs and penicillin
Natural remedy
believed by some are
natural cherries